CALCITONIN-GENE-RELATED PEPTIDES MODULATE THE ACUTE INFLAMMATORY RESPONSE INDUCED BY INTERLEUKIN-1 IN THE MOUSE
CALCITONIN-GENE-RELATED PEPTIDES MODULATE THE ACUTE INFLAMMATORY RESPONSE INDUCED BY INTERLEUKIN-1 IN THE MOUSE
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DOI：
10.1016/0014-2999(94)00503-6
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发表时间：
1994-11-03
影响因子：
5
通讯作者：
PERRETTI, M
中科院分区：
文献类型：
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作者：
AHLUWALIA, A;PERRETTI, M
白细胞介素-1 β（1和5 ng）在4 h时间点产生中性粒细胞向6日龄小鼠气囊的强烈迁移。内源性降钙素基因相关肽（CGRP）被发现作为介导白细胞介素-1 β（5 ng）诱导的迁移，因为CGRP受体拮抗剂，CGRP-（8-37），减弱细胞反应。两种剂量的白细胞介素-1 β诱导的多形性白细胞积聚也被外源性添加的CGRP增强，这是一种被CGRP-（8-37）阻断的反应。通过测量I-125-白蛋白的渗漏，评估白细胞介素-1 β也导致血浆蛋白外渗到袋中。尽管血浆蛋白质外渗被CGRP增强，这一作用也被CGRP-（8-37）的共同施用所消除，但拮抗剂对单独由细胞因子诱导的血浆外渗没有作用。这些结果表明，内源性CGRP参与介导细胞反应，但不介导白细胞介素-1 β引起的血浆蛋白外渗，并指出CGRP受体的异质性。
Interleukin-1 beta (1 and 5 ng) produced an intense migration of neutrophils into a 6-day-old murine air-pouch at 4 h time-point. Endogenous calcitonin gene-related peptide (CGRP) was found to be involved as a mediator of interleukin-1 beta (5 ng)-induced migration, since the CGRP receptor antagonist, CGRP-(8-37), attenuated the cellular response. The polymorphonuclear leukocyte accumulation induced by both doses of interleukin-1 beta was also potentiated by exogenously added CGRP, a response blocked by CGRP-(8-37). Interleukin-1 beta also caused plasma protein extravasation into the pouch as assessed by measuring leakage of I-125-albumin. Whereas plasma protein extravasation was potentiated by CGRP, again an effect abolished by co-administration of CGRP-(8-37), the antagonist had no effect upon the plasma extravasation induced by the cytokine alone. These results suggest that endogenous CGRP is involved in mediating the cellular response but not plasma protein extravasation evoked by interleukin-1 beta and point to CGRP receptor heterogeneity.